Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Androgenic disorders are those conditions in women characterized by excessive androgen action. They are the most common endocrinopathy of women, affecting from 10% to 20%. Signs are: persistent acne, hirsutism and androgenic alopecia, which is the female equivalent of male pattern baldness. A subgroup, those traditionally labeled as having polycystic ovary syndrome (PCOS), additionally have anovulation, as well as menstrual abnormalities and, often, obesity. Although women with androgenic disorders usually present themselves for help with the skin or menstrual changes, there are other important implications regarding their health. Women with PCOS have varying degrees of insulin resistance, and an increased incidence of Type II diabetes mellitus, as well as unfavorable lipid patterns. The presence of these risk factors is suggested by upper segment obesity, darkening of the skin, and the other skin changes that make up acanthosis nigricans. Diagnosis involves measurement of circulating androgens (of which free testosterone is most important), together with prolactin and FSH when menstrual dysfunction is present. Many women with androgenic skin changes have normal serum androgen levels, suggesting increased end organ sensitivity to androgens. Others have hyperandrogenism (of ovarian or adrenal origin). Treatment is usually successful in controlling acne, reducing hirsutism and stabilizing, or partially reversing, androgenic alopecia. Pharmacological approaches involve suppressing androgen levels, for example, the use of an appropriate oral contraceptive, or antagonizing androgen action with several medications that have this activity. Unfortunately, most women with androgenic disorders are frustrated in their efforts to obtain medical help. Understanding androgenic disorders will enable the physician to significantly help the majority of women with these conditions.
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PMID:Androgens and women's health. 960 8

Obesity is an important factor predisposing to type 2 diabetes mellitus, especially for postmenopausal women. Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour. The aim of the study was to evaluate their possible relationships in obese and diabetic women. Three groups of postmenopausal women (FSH > 30 mIU/ml) were evaluated: 8 diabetic (mean age 56.6 +/- 6.9 y, BMI 29.8 +/- 5.3 kg/m2), 10 obese non-diabetic (mean age 49.6 +/- 5.4 y, BMI 36.0 +/- 3.7 kg/m2) and 12 non-diabetic controls (mean age 52.7 +/- 3.5 y, BMI 27.3 1.9 kg/m2). For each patient BMI and WHR were measured and calculated. Blood samples were collected at 8:00 a.m. after an overnight fast. Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits. Mean plasma NPY concentration was significantly higher in diabetic women than in controls (190.1 pg/ml +/- 85.4 vs 120.4 +/- 36.6). Compared to controls, mean plasma leptin level was significantly higher in obese non-diabetic women (32.9ng/ml +/- 9.2 vs 18.9 +/- 9.1). No significant differences were found between obese non-diabetic and diabetic women. In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001). In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found. In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022). Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.
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PMID:Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus. 1099 41

It is known that the prevalence of cardiovascular diseases, hypertension, noninsulin dependent diabetes mellitus and dyslipidemia in the late adulthood are in connection with intrauterine retardation, characterized by low birth weight. One possible explanation of this phenomenon is the abnormality of hypothalamus-hypophysis-adrenal cortex axis due to the accelerated growth. The authors investigated the steroid levels of young adults; whom birth weight were under 2500 g, and examined the relationship between hormone levels and some parameters of glucose metabolism and cardiovascular system. 75 subjects (43 female and 32 male patients, mean age: 19.6 and 19.8 years, respectively; range 18-22 ys) with low birth weight and without any sign of chronic disease, and 30 healthy, age-matched controls with normal birth weight were investigated. The basal serum cortisol, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), androstenedione (AD), 17-hydroxyprogesterone (17OHP), estradiol (OE), sex-hormone binding globulin (SHBG), FSH, LH and insulin levels were determined. Moreover, oral glucose tolerance test with 75 g glucose (OGTT), impedance cardiography as well as ambulatory blood pressure monitoring were done by all subjects. In both sexes in subjects with low birth weight the mean serum cortisol level was significantly higher, than in the normal controls. In female patients the serum DHEA, DHEAS, AD, and 17OHP levels were significantly higher than in the controls. Moreover, among these females a relationship was found between the elevations of adrenal and gonadal steroids and hyperinsulinemia, characterized by increased insulin response during OGTT. In male subjects a significant correlation was found between serum cortisol levels and systolic blood pressure and heart rate. In females there was a positive relationship between serum DHEA and heart rate. Summarized, the basic abnormality in patients with low birth weight seems to be a relative hypercortisolism, and in females because of hyperinsulinemia exists a mild hyperandrogenism as well. The hypercortisolism may cause cardiovascular abnormalities in males directly, while in females indirectly through the hyperinsulinemia and hyperandrogenism. These subtle abnormalities can be detected when no clinical signs present themselves, in young adulthood, giving the opportunity of taking preventive actions.
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PMID:[Low birth weight, adrenal and sex hormones and their correlation with carbohydrate metabolism and cardiovascular physiology, investigated in young adulthood] . 1103 33

Hypoandrogenemia is frequently associated with hyperinsulinemia in men with the metabolic syndrome. We questioned whether insulin or changes in blood glucose levels influence pituitary gonadotropin secretion or testicular steroidogenesis in healthy men. Also, the relationship between hypoglycemia-induced activation of the hypothalamus-pituitary-adrenal axis and altered steroidogenesis was examined. Euglycemic and hypoglycemic clamp experiments were performed in 30 healthy men over a period of 6 h. Half of the men were infused with insulin at a rate of 1.5 mU/min.kg; the other half were infused at a rate of 15.0 mU/min.kg. Plasma glucose was held constant during a euglycemic clamp session and was decreased stepwise in a hypoglycemic clamp session. LH and total/free T concentrations decreased under hypoglycemic conditions regardless of the rate of insulin infusion. With euglycemic conditions, LH and T levels remained unchanged. Dehydroepiandrosterone concentrations increased during hypoglycemia, but not during the euglycemic conditions. The FSH concentration was not affected by insulin or glycemic clamps. Hypoglycemia acutely suppresses T secretion, and this effect is apparently mediated by pituitary LH. Insulin is ineffective. As counterregulation to hypoglycemia begins at normoglycemic ranges in poorly controlled type 2 diabetes and probably also in patients with long-term perturbed glucose regulation in the metabolic syndrome, control of glucose-responsive neurons in the brain may contribute to hypoandrogenemia. Apart from down-regulation of hypothalamic release of GnRH, concurrent activation of the pituitary-adrenal axis (i.e. increased release of dehydroepiandrosterone) may add to the suppressive effect of hypoglycemia on gonadal steroidogenesis.
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PMID:Hypoglycemia, but not insulin, acutely decreases LH and T secretion in men. 1160 May 62

A 46-year-old Japanese male was admitted for the evaluation of severe hypertension. He was obese and had a eunuchoidal body habitus. Chromosomal analysis revealed a 46, XY/47, XXY karyotype. Serum LH, FSH and testosterone levels were low, indicating hypogonadotropic hypogonadism. Endocrinological dynamic tests disclosed presence of hypothalamic panhypopituitarism, partial diabetes insipidus, type 2 diabetes mellitus and low renin essential hypertension. Brain computed tomography and magnetic resonance imaging revealed intra- and extrasellar masses. Histological examination of the tissue obtained at transsphenoidal surgery showed a Rathke's cleft cyst (RCC). To the best of our knowledge, this is the first case report of mosaic Klinefelter's syndrome accompanied by symptomatic RCC, type 2 diabetes mellitus and low renin essential hypertension.
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PMID:Multiple endocrine disorders and Rathke's cleft cyst with Klinefelter's syndrome: a case report. 1240 86

The case of a 62-year-old woman with severe post-menopausal hirsutism is described. Her clinical history revealed regular menstrual periods until menopause at the age of 50, hysterectomy for fibromatosis at 58 years, non-insulin dependent diabetes mellitus, hypertension, obesity, severe hirsutism, which had developed in the previous 3 years, with a deeping of the voice. Examination showed android obesity, hypertension and severe hirsutism involving the face and the trunk. Endocrine evaluation pointed out regular adrenal function, serum total and free-testosterone in the adult male range, with normal androstenedione, DHEAS and 17OHP levels. Estradiol was slightly increased and LH and FSH were inappropriately low for her post-menopausal age. Computed tomography of the abdomen showed regular adrenal glands, and a radio-labeled cholesterol scan was negative. A further pelvic transvaginal ultrasonography revealed a small cystic formation near the right ovary and a slight increase in the size of the left ovary. The patient underwent bilateral ovariectomy. Histological examination showed a lipoid cell tumor within the left ovary. Immunohistochemical studies were positive for inhibin and cytokeratin. After surgery, serum testosterone fell to normal levels, gonadotropins increased to menopausal levels, confirming that the tumor was able to produce both LH, and FSH-inhibiting factors, and hirsutism greatly improved. Periodic hormonal tests remained normal and CT of the abdomen and pelvic ultrasonography did not show alterations at a 3 years follow-up.
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PMID:[Severe postmenopausal hyperandrogenism due to an ovarian lipoid cell tumor: a case report]. 1525 55

Type 2 diabetes is associated with lower total testosterone (T) levels in cross-sectional studies. However, it is not known whether the defect is primary or secondary. We investigated the prevalence of hypogonadism in type 2 diabetes by measuring serum total T, free T (FT), SHBG, LH, FSH, and prolactin (PRL) in 103 type 2 diabetes patients. FT was measured by equilibrium dialysis. FT was also calculated by using T and SHBG (cFT). Hypogonadism was defined as low FT or cFT. The mean age was 54.7 +/- 1.1 yr, mean body mass index (BMI) was 33.4 +/- 0.8 kg/m(2), and mean HbA1c was 8.4 +/- 0.2%. The mean T was 12.19 +/- 0.50 nmol/liter (351.7 +/- 14.4 ng/dl), SHBG was 27.89 +/- 1.65 nmol/liter, and FT was 0.250 +/- 0.014 nmol/liter. Thirty-three percent of patients were hypogonadal. LH and FSH levels were significantly lower in the hypogonadal group compared with patients with normal FT levels (3.15 +/- 0.26 vs. 3.91 +/- 0.24 mIU/ml for LH and 4.25 +/- 0.45 vs. 5.53 +/- 0.40 mIU/ml for FSH; P < 0.05). There was a significant inverse correlation of BMI with FT (r = -0.382; P < 0.01) and T (r = -0.327; P < 0.01). SHBG correlated inversely with BMI (r = -0.267; P < 0.05) but positively with age (r = 0.538; P < 0.001) and T (r = 0.574; P < 0.001). FT correlated strongly with cFT (r = 0.919; P < 0.001) but not with SHBG. LH levels correlated positively with FT (r = 0.287; P < 0.05). We conclude that hypogonadotropic hypogonadism occurs commonly in type 2 diabetes.
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PMID:Frequent occurrence of hypogonadotropic hypogonadism in type 2 diabetes. 1575 66

By screening 204 diabetes patients, a male with age 38 was found to have increased C-peptide levels in plasma (over 6 ng/ml) and urine (430 microg/day), both of which were the highest among the screened subjects. He developed type 2 diabetes at age 31, without history of obesity (weight was 52 kg and height 170 cm). He had bilateral testicular atrophy. Fasting plasma glucose level was 160 mg/dl and HbA1c was 8% at age 38. There was hypertriglycemia (290-662 mg/dl). There were no abnormal peaks of IRI or CPR in the serum fractionated by gel filtration (Biogel P 30). Molar ratio of p-CPR/s-IRI was 10.8. Islet cell antibody, anti-insulin binding antibody and anti-insulin receptor antibody were negative. LSH and FSH were both elevated, and free testosterone was decreased. TSH and Leptin levels were elevated. Other laboratory data were within normal range. CT scan revealed fatty liver and horse-shoe kidney. These clinical pictures do not match the criteria to known syndromes associated with diabetes. Although the single case report is insufficient to discuss the C-peptide mechanism of action, this case may give us a hint to understand an aspect of the pathophysiology of C-peptide's bioactivity dysfunction.
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PMID:A case of type 2 diabetes with high levels of plasma and urinary C-peptide. 1556 62

Expression of the diabetes (db/db) mutation in C57BL/KsJ mice suppresses the female pituitary-gonadal axis via progressive cytolipidemic disruption of hypophyseal gonadotropin release, culminating in premature involution of the reproductive tract and manifest infertility. The current studies define the systemic, endocrine, cytochemical and structural apoptotic changes that result from pituitary hypercytolipidemia induced by db/db mutation expression in this Type II diabetes-obesity syndrome (DOS) model. Adult female C57BL/KsJ control (+/? genotype) and db/db littermates were monitored for systemic and cellular alterations in LH-, FSH- and gonadal steroid-secretion, and coincident pituitary apoptosis, as indexed by TUNEL labeled 3' nuclear DNA-fragmentation, associated with cytolipid depositions. Obesity, hyperglycemia and hyperinsulinemia characterized all db/db-mutants relative to +/? groups. Serum progesterone (P) and estradiol (E2) concentrations were suppressed in db/db mutants coincident with decreased plasma LH and FSH concentrations relative to +/? values. Cytochemical analysis of anterior (AP) pituitary cell subtypes indicated that db/db mutants demonstrated prominent hypercytolipidemia relative to +/? pituitary cytoarchitecture. Cytolipidemic vacuoles were localized within protein vesiculated db/db hypophyseal basophilic and acidophilic cell populations. Hypophyseal cytoadiposity in db/db AP cells was co-localized with prominent cellular apoptotic TUNEL labeling of nuclear 3'-DNA fragments in cells demonstrating vesicular depopulation and cytolytic vacuolization. These data represent the first demonstration of co-localized hypercytolipidemic and cytoapoptotic disruptive events occurring concurrently in a hypopituitary-hypogonadal syndrome model following expression of the Type II (NIDDM) diabetes-obesity syndrome in db/db-mutants. The coincident and progressive vascular-, interstitial- and cyto-lipidemic alterations in hypophyseal cytoarchitecture correlated with the concurrent apoptotic disruption of pituitary endocrine cytoarchitecture and supressed gonadal steroid synthesis, influences which collectively contribute to the premature involution of the pituitary-gonadal axis in C57BL/KsJ- db/db mice.
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PMID:Hypophyseal lipoapoptosis: diabetes (db/db) mutation-associated cytolipidemia promotes pituitary cellular disruption and dysfunction. 1563 92

Pituitary apoplexy is an acute clinical event usually caused by hemorrhage or infarction in a pituitary adenoma. We report the unusual case of hemorrhagic pituitary apoplexy in an 18 year-old male with previously undiagnosed type 2 diabetes mellitus who presented with unexplained hyperglycemia (glucose 49.2 mmol/l [887 mg/dl]) and obtundation and in whom an initial diagnosis of non-ketotic hyperglycemic coma (NKHC) was made. MRI revealed a heterogeneous mass arising from an expanded sella turcica into the suprasellar cistern. Despite well-controlled glucose levels on continuous insulin infusion, dexamethasone, and initiation of bromoergocriptine (parlodel) therapy, the patient's vision and pupillary responses deteriorated acutely. Following emergency transphenoidal surgery, the patient's vision and mental status improved. Data confirmed preoperative panhypopituitarism; serum prolactin was 396 ng/ml (microg/l). Immunostudies demonstrated tumoral labeling for prolactin, but not for ACTH, GH, TSH, LH, FSH, or P53.
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PMID:Hemorrhagic pituitary apoplexy in an 18 year-old male presenting as non-ketotic hyperglycemic coma (NKHC). 1604 31


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